Analysis of etching mechanism and etched slope control of silicon for nanoimprinting lithography.

In the nanoimprint lithography (NIL) process, profile control of imprint masters is a very important task. Therefore, we attempted to control the etched slope of imprint masters as a function of adding O2 to CF4 plasma. Etched profile mechanisms and relationships between the etch kinetics and plasma chemistry were explored using zero-dimensional-based modeling. O2 flow rate increased to 24 sccm, the Si etch rate increased in the range of 186-393 nm/min, while the etch rate rapidly decreased as the O2 flow rate increases beyond 24 sccm. Meanwhile, change in the etch rate of SiO2 followed a similar tendency as the etch rate of Si as a function of O2 flow rate in the CF4/O2 mixing gases. The Si and SiO2 etch rate were expected to be closely dependent on the F radical intensity in CF4/O2 mixing gases. Moreover, the results of simulated normalized lateral etch critical dimension (NLECD) are in agreement with the measured NLECD as a function of O2 flow rate in the CF4/O2 mixing gases.

Induction of apoptosis in p53-deficient human hepatoma cell line by wild-type p53 gene transduction: inhibition by antioxidant.

We investigated the role of wild-type (wt)-p53 as an inducer of apoptotic cell death in human hepatoma cell lines. Following the retrovirus-mediated transduction of the wt-p53 gene, Hep3B cells lacking the endogenous p53 expression began to die through apoptosis in 4 h. They showed a maximal apoptotic death at 12 h, whereas HepG2 cells expressing endogenous p53 did not. However, the transduction of the wt-p53 gene elicited growth suppression of both Hep3B and HepG2 cells. P21(WAF1/CIP1), a p53-inducible cell cycle inhibitor, was induced, not only in Hep3B cells undergoing apoptosis, but also in HepG2 cells. The kinetics of the p21(WAF1/CIP1) induction, DNA fragmentation, and growth suppression of the Hep3B cells showed that DNA fragmentation and growth suppression progressed rapidly following p21(WAF1/CIP1) accumulation. N-acetyl-cysteine or glutathione, potent antioxidants, strongly inhibited the DNA fragmentation, but did not reduce the elevated level of p21(WAF1/CIP1). These findings suggested that p21(WAF1/CIP1) was not a critical mediator for the execution of p53-mediated apoptosis, although it contributed to the growth inhibition of cells undergoing apoptosis. Furthermore, p53-mediated apoptosis could be repressed by antioxidants.